{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:53:50Z","timestamp":1791140030707,"version":"4.1.0"},"reference-count":37,"publisher":"Microbiology Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,5,1]]},"abstract":"<jats:p>Transcriptional profiling data accumulated in recent years for the clinically relevant pathogen <jats:italic>Staphylococcus aureus<\/jats:italic> have established a cell wall stress stimulon, which comprises a coordinately regulated set of genes that are upregulated in response to blockage of cell wall biogenesis. In particular, the expression of <jats:italic>cwrA<\/jats:italic> (SA2343, N315 notation), which encodes a putative 63 amino acid polypeptide of unknown biological function, increases over 100-fold in response to cell wall inhibition. Herein, we seek to understand the biological role that this gene plays in <jats:italic>S. aureus. cwrA<\/jats:italic> was found to be robustly induced by all cell wall-targeting antibiotics tested \u2013 vancomycin, oxacillin, penicillin G, phosphomycin, imipenem, hymeglusin and bacitracin \u2013 but not by antibiotics with other mechanisms of action, including ciprofloxacin, erythromycin, chloramphenicol, triclosan, rifampicin, novobiocin and carbonyl cyanide 3-chlorophenylhydrazone. Although a \u0394<jats:italic>cwrA S. aureus<\/jats:italic> strain had no appreciable shift in MICs for cell wall-targeting antibiotics, the knockout was shown to have reduced cell wall integrity in a variety of other assays. Additionally, the gene was shown to be important for virulence in a mouse sepsis model of infection.<\/jats:p>","DOI":"10.1099\/mic.0.036129-0","type":"journal-article","created":{"date-parts":[[2010,2,19]],"date-time":"2010-02-19T01:45:19Z","timestamp":1266543919000},"page":"1372-1383","source":"Crossref","is-referenced-by-count":35,"title":["cwrA, a gene that specifically responds to cell wall damage in Staphylococcus aureus"],"prefix":"10.1099","volume":"156","author":[{"given":"Carl J.","family":"Balibar","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases, Novartis Institutes for BioMedical Research, 500 Technology Square, Cambridge, MA 02139, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyu","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, Novartis Institutes for BioMedical Research, 500 Technology Square, Cambridge, MA 02139, 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